EyeWorld Asia-Pacific September 2014 Issue

25 EWAP GLAUCOMA September 2014 mercury and the other 50% lowers it just 2 or 3, or a drug that always lowers the pressure 5 or 6 mm Hg?” Dr. Simmons said. “I would Tina WONG, BSc(Hons), MBBS, FRCOphth, FRCS(Ed), FAMS, PhD(Lond) Associate Professor and Senior Consultant, Glaucoma Service, Singapore National Eye Centre 11 Third Hospital Avenue, Singapore 168751 Tel. no. +65-63228131 tina.wong.t.l@snec.com.sg T o glaucomacologists and their patients, there are now exciting developments in the pipeline that will bring new alternatives to current medical therapies. We can look forward to a potential new class of drug that may be the next wonder drug to supersede the prostaglandins, which have reigned as the most successful pressure lowering drugs for the past two decades. Rho kinase inhibitors are emerging as a new kid on the block, targeting the trabecular meshwork to increase outflow facility. Another new drug candidate, FPEP3, claims to have dual action in increasing uveoscleral and trabecular outflow. All eyes will be on the clinical evaluation of these exciting new classes of drugs. We also can look toward new and improved formulations of prostaglandins that are preservative free, which will be a relief for those patients who are sensitive to preservative-containing medications. Finally, we mustn’t forget the efforts in developing sustained drug release formulations to deliver drugs over several months. Patient noncompliance will be greatly reduced, and quality of life improved through the application of such delivery systems in glaucoma medical management. However, both the safety and the efficacy of these systems compared to existing eyedrop treatments will need to be proven and not compromised for such new treatment modalities to be accepted. A considerable amount of effort continues in the development of better treatments for glaucoma. It is clear from this that medical therapy remains an important tool for treating glaucoma, and the options that will be available to patients will increase with these new emerging products. Editors’ note: Dr. Wong holds a patent for a sustained drug delivery system for glaucoma and is co-founder of a company involved in its commercial development. considered is the FPEP3 dual receptor agonists. One being developed by Ono Pharmaceuticals (Osaka, Japan) is under investigation for hypertension or early glaucoma. “It appears to increase both trabecular and uvealscleral outflow,” Dr. Bacharach said. “These are early studies, but it suggests that this novel agent is effective at lowering pressure.” Dr. Bacharach is an investigator for a medication with a new spin on latanoprost—latanoprostene bunod (Bausch + Lomb, Bridgewater, NJ, U.S.), which has a backbone of latanoprost and a nitric oxide- donating side chain. This new formulation is supposed to increase the efficacy of latanoprost, Dr. Bacharach explained. Currently there are two separate trials going on involving this agent, one dubbed APOLLO and the other LUNAR. These are designed to compare the efficacy and safety of the test molecule latanoprostene bunod administered once daily to timolol 0.5% giventwice daily. “The phase 2 studies were complete and latanoprostene bunod met its primary efficacy endpoint and showed positive results on a number of secondary endpoints as well, consistently lowering IOP in a dose-dependent manner,” Dr. Bacharach said. When compared to latanoprost, latanoprostene bunod also did better. “All 4 test doses showed greater IOP reduction compared to latanoprost, with the difference for 2 of the 4 doses reaching more than 1mm,” he said. “The most common adverse event was ocular hyperemia, which occurred at a similar rate in all treatment argue you would rather have the latter.” Jason Bacharach, MD , medical director, Northbay Eye Associates, Sonoma County, Calif., U.S., and co-director of the glaucoma division, California Pacific Medical Center, San Francisco, Calif., U.S., explained that the Rho-kinases work differently than the current gold standard prostaglandins. “Rho- kinase works on the trabecular outflow pathway while the prostaglandins primarily work on uveal scleral outflow,” Dr. Bacharach said. One of the Rho-kinase inhibitors, AR13324 (Aerie Pharmaceuticals, Bedminster, NJ, U.S.), has an additional mechanism. “It’s not just the Rho-kinase inhibition, it also has a norepinephrine transporter,” he said. “The Rho-kinase increases trabecular outflow and the norepinephrine transporter decreases aqueous production, so you get a combination effect. At the 2014 American Glaucoma Society meeting, Dr. Bacharach presented results of a trial comparing AR13324 to latanoprost. “It was effective and well tolerated in patients with glaucoma and ocular hypertension,” he said of the new Rho-kinase inhibitor. L. Jay Katz, MD , director of the glaucoma service, Wills Eye Hospital, Philadelphia, Pa., U.S., pointed out that the Rho-kinase inhibitors may be synergistic with latanoprost. “The Rho-kinase inhibitors in particular improve trabecular meshwork outflow, so you would think that with a drug like prostaglandins that would be good because those drugs improve uveal scleral outflow,” Dr.Katz said. Dr. Bacharach noted that another class of agents being continued on page 27